We studied the usefulness of Kremezin, an oral sorbent, in managing renal failure in diabetic patients, treating 28 diagnosed clinically with diabetic nephropathy to progressive renal failure with 2.4-6g/day of Kremezin for 6 months. Changes in serum creatinine (Cr) and other parameters were compared before and after treatment, with the following results:(1) Cr increase was blunted in 65.4%.(2) The mean slope of the I/Cr-time curve (dl/mg.week) was-0.0043 before and-0.0015 after treatment, indicating a significant reduction in steepness after treatment.(3) Maintenance doses of 6g (n=14) and 3 g (n=14) were compared. In the group with a daily dose of 6g, the steepness of the gradient was significantly reduced from-0.0050 before to-0.0011 after treatment.In the group with a dose of 3g, although the slope tended to become less steep after treatment, the difference was not significant.(4) Indoxyl sulfate was significantly lowered from 0.53±0.50mg/dl before to 0.34±0.40mg/dl after treatment in the 6g dosage group but did not change significantly in the 3g dosage group.These results indicate the beneficial effects of Kremezin for renal failure in diabetic patients. Kremezin administered at a daily dose of 6 g effectively blunts progression to renal failure in diabetic patients with chronic diabetic renal failure.

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We conducted glucose tolerance tests and measured systolic blood pressure (SBP), diastolic blood pressure (DBP), serum cholesterol (T-Chol), and body mass index (BMI) in a rural population in 1991, then reexamined them in 1996. Of the 1, 374 in 1991 participants, 776 (56.5%) participated in 1996. In 1991, 44 were classified with diabetes mellitus (DM), 140 with impaired glucose tolerance (IGT), and 592 as normal (N). We classified risk factors into 2 categories (H-BP: SBP>=140 or DBP>=90, H-SBP: SBP>=140, H-DBP: DBP>=90, H-TC: TChol>=220, H-BMI: BMI>=24) using 1991 information. The relationship between changes in glucose intolerance in the 5-year interval and these factors were expressed by an odds ratio (OR) controlled for age and gender. Logistic regression analysis is used to calculate OR. Previous historyis of HBMI (OR=2.26, 95% CI=1.56-3.28) and H-DBP (OR=1.91, 95%CI=1.08-3.36) were statistically significant factors related to changes in glucose intolerance over the 5 years.

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We report a 48-year-old man with diabetes mellitus harboring mutation in mitochondrial DNA complicated by Usher syndrome. The patient reported a history of visual field loss at age 18, bilateral sensorineural deafness at age 28, and diabetes at age 35. He took medication for diabetes from age 40. At the end of February 1999, his hearing suddenly worsened and he was admitted for therapy. He had bilateral cataracts and advanced retinitis pigmentosa, making him almost blind. Audiography showed a decrease in hearing capacity to 115dB, in the left ear and 78.3dB. in the right ear. HbA1c was 9.5%. Urinary CPR excretion was 15gμ/day, and ΔCPR was 0.8ng/ml in glucagon load testing, suggesting decreased in insulin secretion.A point mutation at position 3243 in mitochondrial DNA was detected in peripheral blood leukocytes. We consider the man to be a rare case with mitochondrial diabetes complicated by Usher syndrome characterized by juvenile-onset retinitis pigmentosa and progressive sensorineural deafness.

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A 35-year-old woman with a 1-year history of type 1 diabetes mellitus (DM) was admitted in December 1997 with dysphagia, deteriorated vision, diplopia, and dyspnea. At age 14 years, Basedow disease had been successfully treated with radioiodine. She was diagnosed as having type 1 DM at age 34, being positive for anti-GAD antibody and (ICA). Neurological examination on admission revealed left oculomotor nerve palsy, optic neuritis, and bulbar palsy. Magnetic resonace imaging (MM) showed multiple high signal intensity (T2) lesions in the midbrain, pons, and medulla oblongata. IgG and myelin basic protein were positive in cerebrospinal fluid, heading to a diagnosis of multiple sclerosis (MS). After admission, she was immediately treated with steroid pulse therapy and her glycemia strictly controlled with continuous subcutaneous insulin infusion, which simultaneously improved both hyperglycemia and anti-GAD antibody titer, in addition to MS. In August 1998, the patient was readmitted with relapsing MS, together with marked elevations of plasma glucose and anti-GAD antibody, all improved with the same treatment as previously, suggesting that autoimmunity and hyperglycemia play important roles in the onset or exacerbation of MS associated with type 1 DM.

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A 68-year-old man was referred to our hospital with diabetes mellitus, exanthema of the legs, and weight loss. He had been diagnosed with diabetes when 46 years old and diet therapy was initiated, but glucose control was poor. He had suffered from intractable exanthema of the lower legs since age 48. Insulin therapy was started when he was 59, after which his exanthema worsened. Close examination on admission showed hypoproteinemia, marked anemia, and a calcified pancreatic tumor in computed tomography (CT) scanning. Plasma pancreatic glucagon (IRG) was 2360pg/ml. After subtotal pancreatectomy with total splenectomy, skin lesions and high IRG disappeared. The tumor was diagnosed immunohistopathologically as glucagonoma. Exanthema in this patient was inconsistent with necrolytic migratory erythema (NME), a pathognomonic symptom of glucagonoma syndrome.
In summary, glucagonoma was found 20 years after diabetes was diagnosed, indicating the difficulty of making a differential diagnosis of skin lesions.

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[in Japanese]

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[in Japanese]

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[in Japanese]

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[in Japanese]

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